Alcohol Use Disorders In Adulthood Research Articles

Evidence of subgroup differences in meta-analyses evaluating medications for alcohol use disorder: An umbrella review.

Randomized controlled trials (RCTs) evaluating medications for alcohol use disorder (AUD) often examine heterogeneity of treatment effects through subgroup analyses that contrast effect estimates in groups of patients across individual demographic, clinical, and study design-related characteristics. However, these analyses are often not prespecified or adequately powered, highlighting the potential role of subgroup analyses in meta-analysis. Here, we conducted an umbrella review (i.e., a systematic review of meta-analyses) to determine the range and characteristics of reported subgroup analyses in meta-analyses of AUD medications. We searched PubMed to identify meta-analyses of RCTs evaluating medications for the management of AUD, alcohol abuse, or alcohol dependence in adults. We sought studies that measured drinking-related outcomes; quality of life, function, and rates of mortality; adverse events; and dropout. We considered meta-analyses that reported the results from formal subgroup analyses (comparing the summary effects across subgroup levels); summary effect estimates stratified across subgroup levels; and meta-regression, regression, or correlation-based subgroup analyses. We analyzed nine meta-analyses that included 61 formal subgroup analyses (median = 6 per meta-analysis), of which 33 (54%) were based on baseline participant-level and 28 (46%) were based on trial-level characteristics. Of the 58 subgroup analyses with either a p-value from a subgroup test or a statement by the authors that the subgroup analyses were not statistically significant, eight (14%) were statistically significant at the p < 0.05 level. Twelve meta-analyses reported the results of 102 meta-regression analyses, of which 25 (25%) identified statistically significant predictors of the relevant outcome of interest; nine (9%) were based on baseline participant-level and 93 (91%) were based on trial characteristics. Subgroup analyses across meta-analyses of AUD medications often focus on study-level characteristics, which may not be as clinically informative as subgroup analyses based on participant-level characteristics. Opportunities exist for future meta-analyses to standardize their subgroup methodology, focus on more clinically informative participant-level characteristics, and use predictive approaches to account for multiple relevant variables.

Comorbidity of anxiety/affective, conduct/antisocial, attention deficit, and alcohol use disorders with suicidal behaviors in an American Indian community sample of adults and adolescents

AimsTo study the associations of anxiety/affective disorders, conduct/antisocial disorders (ASPD/CD), attention deficit disorders (ADHD), and alcohol use disorders (AUD) with suicidal behaviors in an American Indian (AI) community sample of adolescents and adults. MethodsParticipants were AI (360 adolescents, 925 adults) recruited from reservations who were assessed with the Semi-Structured Assessment for the Genetics of Alcoholism (SSAGA). ResultsAmong AI adults (mean age = 33 years), 17% percent reported lifetime experiences of suicidal thoughts (ideation and/or plans) and 14% reported suicidal acts (including either a suicide attempt history or verified death by suicide; n = 19 deaths). Among AI adolescents (mean age = 15 years), 20% experienced suicidal thoughts and 9% experienced suicidal acts (including 3 deaths). In logistic regression analyses, suicidal thoughts were significantly associated with lifetime diagnoses of affective disorder, CD and ADHD in adolescents, and with anxiety disorder, affective disorder, and ASPD/CD in adults. Suicidal acts were associated with affective disorder, ADHD, and alcohol drinking in adolescents and with anxiety disorder, ASPD/CD and AUD in adults. The number of comorbid disorders greatly increased the risk of both suicidal thoughts and acts among both adolescents and adults. ConclusionsIn addition to affective disorders, both ADHD and CD in adolescents, and ASPD in adults, demonstrated an association with suicidal thoughts. Alcohol use by adolescents and AUD among adults also were associated with suicidal attempts in this AI sample. These findings suggest need for additional research and potential integration of alcohol in screening and intervention programs focused on the prevention of suicide among AI.

Neurocognitive Recovery in Abstinent Patients with Alcohol Use Disorder: A Scoping Review for Associated Factors.

Studies have reported inconsistent results regarding the extent to which neurocognitive recovery occurs in abstinent patients with alcohol use disorder (AUD). In addition to abstinence, other factors may have influenced this process and contributed to the inconsistencies. This review examines the factors investigated in this regard and describes the possible influence of each factor based on the evidence collected. PubMed was systematically searched for articles published between January 2000 and July 2023. Longitudinal humane studies investigating neurocognitive recovery in abstinent adult AUD patients were included. Studies with a cross-sectional design were excluded, as were studies that did not classify AUD according to the DSM-IV or 5 criteria, only examined binge use, did not report neuropsychological outcomes or duration of abstinence, or where neurological disorders were present. Sixteen categories of factors were distinguished from 31 full-text articles. Consistent patterns were found, indicating an association between neurocognitive recovery and the "smoking" and 'brain volume" factors. Consistent patterns were also found indicating that there is no relationship with "quantities of alcohol used" and "education level." A similar consistent pattern was also found for "polysubstance use", "gender" and "verbal reading", but the number of studies is considered limited. The association with "age" is studied frequently but with inconsistent findings. The remaining eight factors were regarded as understudied. The clearest patterns emerging from the evidence are a predominantly negative influence of smoking on neurocognitive recovery, associations between changes in brain area volume and neurocognitive recovery, and no association between neurocognitive recovery and the amount of alcohol consumed, as measured by self-report, nor with educational attainment. Future research on the understudied factors and factors with inconsistent evidence is needed, preferably through longitudinal designs with multiple assessment periods starting after at least two weeks of abstinence.

Effects of adolescent ethanol exposure on adult nondrug reward seeking behavior in male and female mice.

Adolescent alcohol use is associated with an increased likelihood of developing an alcohol use disorder in adulthood, potentially due to the effects of alcohol exposure on reward-seeking behavior. However, it remains unclear whether adolescent drinking is sufficient to alter nondrug reward seeking in adulthood. As adolescence is a period of both brain and sexual maturation, which occur in a sex-dependent manner, males and females may be differentially sensitive to the consequences of adolescent alcohol exposure. The present study investigated whether adolescent ethanol exposure affected food reward taking and seeking in male and female adult mice. Male and female C57BL/6J mice underwent intermittent ethanol exposure (AIE) via vapor inhalation during early adolescence (28-42 days of age). At 10 weeks of age, the mice were trained in a conditioned place preference paradigm (CPP) for a food reward. We measured food consumption, CPP, and cFos expression in multiple brain regions following CPP testing. Data were analyzed using repeated measures analysis of variance with exposure (air vs. AIE), sex, and time as factors. AIE exposure increased food consumption during CPP training in adult male mice, but reduced pellet consumption in adult female mice. AIE exposure impaired CPP expression only in female mice. Despite these behavioral differences, exposure to the reward-paired chamber did not induce differential cFos expression following CPP testing in the prelimbic and infralimbic cortices or the nucleus accumbens core and shell. These findings indicate that adolescent ethanol exposure disrupted nondrug reward taking and seeking in adulthood in female mice and altered consumption in adult male mice.

의사결정나무분석을 이용한 성인의 알코올사용장애 위험요인

Objectives: The aim of this study was to identify risk factors of alcohol use disorder among Korean adults. Methods: Cross-sectional exploratory study based on data collected from Data from the 6th Korea National Health and Nutrition Examination Survey in 2015 were performed in this study. There were 3,248 participants who were 2,558 normal drinkers while 690 had alcohol use disorder. Decision tree analysis were used to exam socio-demographic and health-related factors to predict alcohol use disorder. Results: As a result of decision tree analysis, the predictive model for factors related to alcohol use disorder in Korean adults presented with 8 pathways. The significant predictors of alcohol use disorder were age, gender, smoking, marital status, and house income. Male smokers whose household income is ‘high’ or ‘low’ are most vulnerable to alcohol use disorders. Conclusions: This study indicates that need to consider health behavior and house income when we practice prevention policies and health education of alcohol use disorder.

The effect of parental alcohol use on alcohol use disorder in young adulthood: Exploring the mediating roles of adolescent alcohol expectancies and consumption.

Parental alcohol use and problems are risk factors for alcohol use disorder (AUD), and these effects may be mediated by adolescent alcohol expectancies and consumption. In the present study, we tested the direct effects of mothers' and fathers' alcohol consumption on young adult AUD, as well as the indirect effects through adolescent maximum alcohol use, alcohol consumption, and alcohol expectancies. Participants were 5160 individuals (49.1% female) and their biological parents from the Avon Longitudinal Study of Parents and Children, a cohort study of children born in southwestern England during 1991 and 1992. Structural equation modeling (SEM) was used to test associations of mothers' and fathers' alcohol use (assessed when children were 12 years old) with age 24 AUD. Potential mediator variables included the maximum number of alcoholic drinks consumed within a 24-h period by age 13.5 and alcohol expectancies and alcohol consumption at ages 17 and 20. Higher maternal and paternal alcohol use were associated with higher levels of alcohol consumption at age 17. Greater alcohol consumption, in turn, was related to a more severe presentation of AUD. The overall indirect effects of mothers' (b = 0.033, 95% confidence interval [CI] = 0.006, 0.059) and fathers' drinking (b = 0.041, 95% CI = 0.018, 0.064) on AUD were modest but significant, and were primarily comprised of adolescent alcohol consumption rather than alcohol expectancies. Our findings underscore the importance of both mothers' and fathers' drinking for the development of alcohol use and problems across adolescence and young adulthood.

Coping strategies as mediating mechanisms between adolescent polysubstance use classes and adult alcohol and substance use disorders

Adolescent polysubstance use is a robust predictor of substance use in adulthood and can be exacerbated by poor coping with stress over time. We examined whether latent classes of adolescents’ polysubstance use predicted alcohol use disorder and substance use disorder diagnoses in adulthood via multiple stress coping strategies. Self-reported frequency of past 3-month alcohol, tobacco, and marijuana use in 792 adolescents (aged 16/17) were used to form latent classes of polysubstance use. Self-reported aggressive, reactive, substance use and cognitive coping strategies (ages 18/19, 22/23, 23/24) were examined as multiple mediators of polysubstance use classes and alcohol use disorder and substance use disorder in adulthood (age 26/27) controlling for demographic covariates. Latent class analysis resulted in High, Experimental, and Low polysubstance use classes. Those in high and experimental polysubstance use classes, compared to those in the low polysubstance use class, had greater use of aggressive and reactive coping strategies, which respectively predicted greater substance use disorder and alcohol use disorder in adulthood. Across all comparisons (high vs low, experimental vs low, and high vs experimental), higher polysubstance use was associated with greater substance use coping, which predicted both alcohol and substance use disorder. Greater polysubstance use, even experimental use, in adolescence is a significant risk factor for developing alcohol use disorder and substance use disorder in adulthood and this occurs, in part, via maladaptive stress coping strategies.

Targeting Persistent Changes in Neuroimmune and Epigenetic Signaling in Adolescent Drinking to Treat Alcohol Use Disorder in Adulthood.

Studies universally find early age of drinking onset is linked to lifelong risks of alcohol problems and alcohol use disorder (AUD). Assessment of the lasting effect of drinking during adolescent development in humans is confounded by the diversity of environmental and genetic factors that affect adolescent development, including emerging personality disorders and progressive increases in drinking trajectories into adulthood. Preclinical studies using an adolescent intermittent ethanol (AIE) exposure rat model of underage binge drinking avoid the human confounds and support lifelong changes that increase risks. AIE increases adult alcohol drinking, risky decision-making, reward-seeking, and anxiety as well as reductions in executive function that all increase risks for the development of an AUD. AIE causes persistent increases in brain neuroimmune signaling high-mobility group box 1 (HMGB1), Toll-like receptor, receptor for advanced glycation end products, and innate immune genes that are also found to be increased in human AUD brain. HMGB1 is released from cells by ethanol, both free and within extracellular vesicles, that act on neurons and glia, shifting transcription and cellular phenotype. AIE-induced decreases in adult hippocampal neurogenesis and loss of basal forebrain cholinergic neurons are reviewed as examples of persistent AIE-induced pathology. Both are prevented and reversed by anti-inflammatory and epigenetic drugs. Findings suggest AIE-increased HMGB1 signaling induces the RE-1 silencing transcript blunting cholinergic gene expression, shifting neuronal phenotype. Inhibition of HMGB1 neuroimmune signaling, histone methylation enzymes, and galantamine, the cholinesterase inhibitor, both prevent and reverse AIE pathology. These findings provide new targets that may reverse AUD neuropathology as well as other brain diseases linked to neuroimmune signaling. SIGNIFICANCE STATEMENT: Adolescent underage binge drinking studies find that earlier adolescent drinking is associated with lifelong alcohol problems including high levels of lifetime alcohol use disorder (AUD). Preclinical studies find the underage binge drinking adolescent intermittent ethanol (AIE) model causes lasting changes in adults that increase risks of developing adult alcohol problems. Loss of hippocampal neurogenesis and loss of basal forebrain cholinergic neurons provide examples of how AIE-induced epigenetic and neuroimmune signaling provide novel therapeutic targets for adult AUD.

Effects of voluntary adolescent intermittent alcohol exposure and social isolation on adult alcohol intake in male rats.

Initiating alcohol use in adolescence significantly increases the likelihood of developing adult alcohol use disorder (AUD). However, it has been difficult to replicate adolescent alcohol exposure leading to increased adult alcohol intake across differing preclinical models. In the present study, differentially housed male rats (group vs. single cages) were used to determine the effects of voluntary intermittent exposure of saccharin-sweetened ethanol during adolescence on adult intake of unsweetened 20% ethanol. Adolescent male rats were assigned to group- or isolated-housing conditions and underwent an intermittent 2-bottle choice in adolescence (water only or water vs. 0.2% saccharin/20% ethanol), and again in adulthood (water vs. 20% ethanol). Intermittent 2-bottle choice sessions lasted for 24h, and occurred three days per week, for five weeks. Rats were moved from group or isolated housing to single-housing cages for 2-bottle choice tests and returned to their original housing condition on off days. During adolescence, rats raised in isolated-housing conditions consumed significantly more sweetened ethanol than rats raised in group-housing conditions, an effect that was enhanced across repeated exposures. In adulthood, rats raised in isolated-housing conditions and exposed to sweetened ethanol during adolescence also consumed significantly higher levels of unsweetened 20% ethanol compared to group-housed rats. The effect was most pronounced over the first five re-exposure sessions. Housing conditions alone had little effect on adult ethanol intake. These preclinical results suggest that social isolation stress, combined with adolescent ethanol exposure, may play a key role in adult AUD risk.

Age of onset and alcohol and cannabis use disorders among Mexican American young adults: Robust substance-specific effects of early use as a risk factor

We investigated the substance-specific and cross-substance risk associated with early onset (before age 15) of drunkenness and cannabis use in the subsequent development of alcohol (AUD) and cannabis use disorder (CUD) in Mexican American young adults. Survival analyses employed Cox proportional hazards models for AUD and CUD, separately. In cross-risk analyses, we modeled estimates for those participants reporting lifetime use of both substances. Early onset of drunkenness and early onset of cannabis use were associated with shorter time to AUD and CUD, respectively, even after accounting for psychiatric disorders. While there were no cross-risk associations, adjusting for psychiatric disorders and early onset cannabis use attenuated the association of early drunkenness with AUD.

Definition matters: assessment of tolerance to the effects of alcohol in a prospective cohort study of emerging adults.

Tolerance to the effects of alcohol is an important element in the diagnosis of alcohol use disorders (AUD); however, there is ongoing debate about its utility in the diagnosis AUD in adolescents and young adults. This study aimed to refine the assessment of tolerance in young adults by testing different definitions of tolerance and their associations with longitudinal AUD outcomes. Prospective cohort study. Australia. A contemporary cohort of emerging adults across Australia (n= 565, mean age = 18.9, range = 18-21 at baseline). Clinician-administered Structured Clinical Interview for DSM-IV Research Version (SCID-IV-RV) assessed for AUD criteria across five interviews, at 6-month intervals over 2.5years. Tolerance definitions were operationalized using survey-type response (yes/no), clinician judgement (SCID-IV-RV), different initial drinking quantity and percentage increase thresholds and average heavy consumption metrics. AUD persistence was operationalized by the number of times AUD was present across the 2.5-year study period (n = 491), and new-onset AUD was operationalized as any new incidence of AUD during the follow-up period (n = 461). The (i) SCID-IV-RV clinician judgement [odds ratio (OR) = 2.50, P= 0.005], (ii) an initial drinking quantity threshold of four to five drinks and 50% minimum increase (OR = 2.48, P= 0.007) and (iii) 50% increase only (OR = 2.40, P= 0.005) were the tolerance definitions more strongly associated with any new onset of AUD throughout the four follow-up time-points than other definitions. However, these definitions were not associated with persistent AUD (Ps > 0.05). Average heavy consumption definitions of tolerance were most strongly associated with persistent AUD (OR = 6.66, P= 0.001; OR = 4.65, P= 0.004) but not associated with new-onset AUD (Ps > 0.05). Initial drink and percentage change thresholds appear to improve the efficacy of change-based tolerance as an indicator for new-onset alcohol use disorder diagnosis in self-report surveys of young adults. When predicting persistent alcohol use disorder, average heavy consumption-based indicators appear to be a better way to measure tolerance than self-reported change-based definitions.

Solitary alcohol use in adolescence predicts alcohol problems in adulthood: A 17-year longitudinal study in a large national sample of US high school students

BackgroundIdentifying risk factors for alcohol use disorder (AUD) is important for public health. The social context of drinking—such as drinking alone—may be an independent and robust early risk marker for AUD symptoms later in life. We evaluated whether solitary alcohol use in adolescence (age 18) and young adulthood (age 23/24) was concurrently associated with binge drinking and prospectively predicted age 35 AUD symptoms, and whether associations differed by sex. MethodsLongitudinal data were from the Monitoring the Future study. Surveys were completed by adolescents in 12th grade at age 18 (1976–2002), young adults at age 23/24 (1981–2008), and adults at age 35 (1993–2019). Analyses included past 12-month alcohol users (n = 4464 for adolescent models; n = 4561 for young adult models). Multivariable regression analyses tested whether adolescent and young adult solitary alcohol use was associated concurrently with binge drinking frequency and prospectively with age 35 AUD symptoms. ResultsSolitary alcohol use in adolescence and young adulthood was associated (a) concurrently with binge drinking and (b) prospectively with increased risk of age 35 AUD symptoms (even after controlling for earlier binge drinking, alcohol use frequency, and sociodemographic covariates). Adolescent solitary alcohol use was associated with age 35 AUD symptoms particularly among females; no interaction was observed between sex and young adult solitary alcohol use in predicting age 35 AUD symptoms. ConclusionsAdolescent and young adult solitary alcohol use was associated with increased adult AUD symptoms above and beyond other risk factors; adolescent female solitary alcohol users were especially at risk.

The bidirectional relationship between anxiety disorders and alcohol use disorders in adults: Findings from a longitudinal population-based study

BackgroundAnxiety disorders (AD) and alcohol use disorder (AUD) frequently co-occur, but the temporal order of the association is unclear. We have determined the association between AD and the presence and first-onset of AUD, and vice versa. MethodsData were used from n = 6.646 participants and four measurement waves (baseline, 3-, 6- and 9-years) of the Netherlands Mental Health Survey and Incidence Study 2 (NEMESIS-2), a cohort study of the Dutch general population aged 18–64 years. AD and AUD were assessed with the Composite International Diagnostic Interview 3.0. Multilevel logistic autoregressive models were controlled for previous-wave AD or AUD, sociodemographics (Model 1), smoking and clinical factors (Model 2). ResultsPeople with AUD had a higher risk of present (OR = 1.65, 95 % CI 1.11–2.43; Model 2) and first-onset (OR = 2.03, 95 % CI 1.17–3.51; Model 2) AD in 3-years follow-up intervals than people without AUD. Vice versa, people with AD also had a higher sociodemographics-adjusted risk of present and first-onset AUD over 3-years follow-up intervals, but these associations attenuated into insignificance after adjustment for smoking and clinical variables.LimitationsFor statistical power reasons we were not able to analyze 9-year follow-up data or distinguish between AD and AUD types. ConclusionsOur results indicate a bidirectional relationship between AD and AUD; especially those with severe AD (medication use, comorbid depression) are at risk of developing AUD. Health care professionals should focus on prevention of AD in AUD patients and prevention of AUD in patients with (more severe) AD. Further research should investigate the mechanisms underlying the observed associations.

Reasons for alcohol use and non-use by underage U.S. autistic youth: A qualitative study.

What is already known about the topic? Hazardous alcohol use is when a person's drinking puts them at increased risk for negative events (e.g. health problems or car crashes). Some studies show that autistic people may be at greater risk for hazardous alcohol use than non-autistic people, while other studies have found that hazardous alcohol use is less common among autistic people than non-autistic people. We need to learn why autistic underage youth choose to drink alcohol or not. The goal of this study was to learn from US autistic youth about their attitudes and behavior related to alcohol. Forty autistic youth aged 16-20 years old were interviewed.What this article adds? Youth described several reasons why they choose to drink alcohol, including feeling like non-autistic people are more accepting when drinking, that it puts them in a less irritable or bored mood, helps them cope with problems, and helps them fit in. Reasons for not drinking alcohol include worries about becoming addicted, medication interactions, not liking the taste, fear of experiencing hangover and other health problems, and concern about acting foolish when drunk.Implications for practice, research, or policy Results reveal that hazardous alcohol use in autistic adults could have its roots in underage experiences that give autistic youth temporary relief from social anxiety, feeling lonely, and challenges with sensory processing. Right now, there are no evidence-based alcohol prevention programs in the United States for autistic people. One or more such programs may be needed. The results from this study could be used to adapt existing programs for non-autistic youth to the unique needs and risk factors of autistic youth.

Gender Differences in the Psychosocial Determinants Underlying the Onset and Maintenance of Alcohol Use Disorder.

A large number of different mechanisms have been linked to Alcohol Use Disorder (AUD), including psychosocial, neurocognitive, affective, and neurobiological factors. Gender has been shown to impact the presentation and progression of AUD; yet, little work has been done to parse the different mechanisms underlying AUD within the lens of gender differences. A review of the literature on adolescence revealed that psychosocial factors, in particular lack of family social support and interactions with peers, drive the onset of alcohol use more strongly in girls relative to boys. However, research done on gender differences in disease progression in adults remains limited. Our gender-specific analysis of the mechanisms underlying AUD in adults revealed that lack of social support was causally linked to negative affect, mental health symptoms, and AUD symptom severity in women, but not men. These novel results suggest that psychosocial factors may play a gender-specific role not only in the onset of use in adolescence, but also in the maintenance of addiction in adults. If confirmed, this suggests the need for investigating gender-specific recovery trajectories. In this perspective piece, we review the literature regarding gender differences in the onset and maintenance of AUD and present original data that support unique risk factors in women.

Impact of Culture, Race, Social Determinants Reflected Throughout New DSM-5-TR

Impact of Culture, Race, Social Determinants Reflected Throughout New <i>DSM-5-TR</i>

Naltrexone moderates the association of alcohol use and affect among adolescent drinkers in daily life.

Naltrexone is an efficacious medication for the treatment of alcohol use disorder in adults. As an opioid receptor antagonist, naltrexone blocks activation of the endogenous opioid system, which is involved in the affectively reinforcing properties of substance use. Few studies, however, have examined the moderating effect of naltrexone on the association between affect and alcohol use. Additionally, most existing research on naltrexone has been with adults in the human laboratory. We conducted a secondary analysis of ecological momentary assessment data from a randomized, double-blinded, placebo-controlled cross-over study that compared naltrexone (50mg/daily) and placebo in 26 adolescents (15 to 19years old) who exhibited problematic drinking patterns. Multilevel models tested whether naltrexone moderated associations of alcohol use with both positive and negative affect (PA, NA). Results indicated that, during naltrexone treatment, greater estimated blood alcohol concentration (eBAC) levels were associated with greater NA further into drinking episodes. In turn, greater NA after the first drink of an episode was associated with reduced subsequent eBAC values during naltrexone treatment. Low PA was also associated with lower subsequent eBAC levels in the naltrexone condition after the first drink. These findings support the idea that naltrexone can disrupt the association between affect and alcohol use, effects that emerge later in drinking episodes. Greater attention to the effects of naltrexone on affect and reinforcement may help to tailor psychotherapy to maximize the benefits of naltrexone. However, in the present study, as most drink reports were in the first 2h of the drinking episode and participants reported affect only at the first three end-drink reports of a drinking episode (limiting the number of drinks reported), we had reduced power to detect effects in the continuation phase. Thus, replication of the findings is needed using a design that assesses the impact of naltrexone across the entire episode.

Hospitalizations for Alcohol and Opioid Use Disorders in Older Adults: Trends, Comorbidities, and Differences by Gender, Race, and Ethnicity.

Background:The prevalence of substance use disorders (SUDs) among adults ages 65 and older has been increasing at a notably high rate in recent years, yet little information exists on hospitalizations for SUDs among this age group. In this study we examined trends in hospitalizations for alcohol use disorders (AUDs) and opioid use disorders (OUDs) among adults 65 and older in the United States, including differences by gender and race/ethnicity.Methods:We used Medicare claims data for years 2007-2014 from beneficiaries ages 65 and older. We abstracted hospitalization records with an ICD-9 diagnostic code for an AUD or OUD. Hospitalization rates were calculated using population estimates from the United States Census. We examined trends in quarterly hospitalization rates for hospitalizations with AUD/OUD as primary diagnoses, and separately for those with these disorders as secondary diagnoses. We also examined comorbidities for those with a primary diagnosis of AUD/OUD. Analyses were conducted for all hospitalizations with AUD/OUD diagnoses, and separately by gender and race/ethnicity.Results:Between the last quarter of 2007 and the third quarter of 2014, AUD hospitalization rates increased from 485 to 579 per million (19%), and OUD hospitalization rates from 46 to 101 per million (120%) and varied by gender (for AUD) and race/ethnicity (for both AUD and OUD). Hospitalization rates were particularly high for Black older adults, as was the increase in hospitalization rates. The increase in hospitalization rates was substantially higher for hospitalizations with AUD (84%) and OUD (269%) as secondary diagnoses.Conclusions:Hospitalizations for AUDs and OUDs among older adults increased at an alarming rate during the observation period, and disparities existed in hospitalization rates for these conditions. Interventions focusing on the needs of older adults with AUD and/or OUD are needed, particularly to address the needs of a growing racially/ethnically diverse older adult population.

Family alcohol use, rather than childhood trauma, is more likely to cause male alcohol use disorder: findings from a case-control study in northern China

ObjectiveTo explore the influence of childhood trauma and family alcohol use on male alcohol use disorder.MethodsWe conducted a case-control study using Childhood Trauma Questionnaire (CTQ) and a structured interview involving 129 men with alcohol use disorder and 129 healthy male volunteers. The two groups were compared in terms of childhood trauma, parental drinking behavior, and attitudes toward childhood drinking.ResultsPatients showed higher scores of CTQ than controls on childhood trauma experiences, including on the subscales of physical abuse, emotional abuse, sexual abuse, and emotional neglect. Higher proportions of patients than controls had fathers who drank seven or more times a week, and had mothers who were opposed to childhood drinking. Conversely, a smaller proportion of patients than controls had fathers who opposed childhood drinking. Patients were more likely than controls to have been induced to drink as children. Logistic regression analysis identified three risk factors for alcohol use disorder: induced drinking during childhood [odds ratio (OR) 6.09, 95% confidence interval (CI) 2.56–14.51], the father’s weekly alcohol consumption during the respondent’s childhood (OR 4.40, 95%CI 2.94–6.58) and history of smoking (OR 3.39, 95%CI 1.48–7.77). Conversely, more years of education were a protective factor against alcohol use disorder (OR 0.88, 95% CI 0.78–0.99).ConclusionsMen whose fathers drank frequently during their childhood and were encouraged to drink may be at increased risk of alcohol use disorder in adulthood. In fact these factors of family alcohol use appear to increase risk of alcohol use disorder among adult men more than exposure to childhood trauma does.

High Polygenic Risk Scores Are Associated With Early Age of Onset of Alcohol Use Disorder in Adolescents and Young Adults at Risk

BackgroundGenome-wide association studies have been conducted in alcohol use disorder (AUD), and they permit the use of polygenic risk scores (PRSs), in combination with clinical variables, to predict the onset of AUD in vulnerable populations. MethodsA total of 2794 adolescent/young adult subjects from the Collaborative Study on the Genetics of Alcoholism were followed, with clinical assessments every 2 years. Subjects were genotyped using a genome-wide chip. Separate PRS analyses were performed for subjects of European ancestry and African ancestry. Age of onset of DSM-5 AUD was evaluated using the Cox proportional hazard model. Predictive power was assessed using receiver operating characteristic curves and by analysis of the distribution of PRS. ResultsEuropean ancestry subjects with higher than median PRSs were at greater risk for onset of AUD than subjects with lower than median PRSs (p = 3 × 10–7). Area under the curve for the receiver operating characteristic analysis peaked at 0.88 to 0.95 using PRS plus sex, family history, comorbid disorders, age at first drink, and peer drinking; predictive power was primarily driven by clinical variables. In this high-risk sample, European ancestry subjects with a PRS score in the highest quartile showed a 72% risk for developing AUD and a 35% risk of developing severe AUD (compared with risks of 54% and 16%, respectively, in the lowest quartile). ConclusionsPredictive power for PRSs in the extremes of the distribution suggests that these may have future clinical utility. Uncertainties in interpretation at the individual level still preclude current application.